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  • Society for Neuroscience  (16)
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  • 1
    Online Resource
    Online Resource
    Arginine Methyltransferase 1 in the Nucleus Accumbens Regulates Behavioral Effects of Cocaine
    Society for Neuroscience ; 2015
    In:  The Journal of Neuroscience Vol. 35, No. 37 ( 2015-09-16), p. 12890-12902
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 35, No. 37 ( 2015-09-16), p. 12890-12902
    Abstract: Recent evidence suggests that histone modifications play a role in the behavioral effects of cocaine in rodent models. Histone arginine is known to be methylated by protein arginine N -methyltransferases (PRMTs). Evidence shows that PRMT1 contributes to 〉 90% of cellular PRMT activity, which regulates histone H4 arginine 3 asymmetric dimethylation (H4R3me2a). Though histone arginine methylation represents a chemical modification that is relatively stable compared with other histone alterations, it is less well studied in the setting of addiction. Here, we demonstrate that repeated noncontingent cocaine injections increase PRMT1 activity in the nucleus accumbens (NAc) of C57BL/6 mice. We, subsequently, identify a selective inhibitor of PRMT1, SKLB-639, and show that systemic injections of the drug decrease cocaine-induced conditioned place preference to levels observed with genetic knockdown of PRMT1. NAc-specific downregulation of PRMT1 leads to hypomethylation of H4R3me2a, and hypoacetylation of histone H3 lysine 9 and 14. We also found that H4R3me2a is upregulated in NAc after repeated cocaine administration, and that H4R3me2a upregulation in turn controls the expression of Cdk5 and CaMKII . Additionally, the suppression of PRMT1 in NAc with lentiviral-short hairpin PMRT1 decreases levels of CaMKII and Cdk5 in the cocaine-treated group, demonstrating that PRMT1 affects the ability of cocaine to induce CaMKII and Cdk5 in NAc. Notably, increased H4R3me2a by repeated cocaine injections is relatively long-lived, as increased expression was observed for up to 7 d after the last cocaine injection. These results show the role of PRMT1 in the behavioral effects of cocaine. SIGNIFICANCE STATEMENT This work demonstrated that repeated cocaine injections led to an increase of protein arginine N -methyltransferase (PRMT1) in nucleus accumbens (NAc). We then identified a selective inhibitor of PRMT1 (SKLB-639), which inhibited cocaine-induced conditioned place preference (CPP). Additionally, genetic downregulation of PRMT1 in NAc also attenuated cocaine-caused CPP and locomotion activity, which was associated with decreased expression of histone H4 arginine 3 asymmetric demethylation (H4R3me2a) and hypoacetylation of histone H3 lysine 9 and 14 (acH3K9/K14). This study also showed that H4R3me2a controlled transcriptions of Cdk5 and CaMKII, and that PRMT1 negatively affected the ability of cocaine to induce CaMKII and Cdk5 in NAc. Notably, increased H4R3me2a by repeated cocaine injection was relatively long-lived as increased expression was observed up to 7 d after withdrawal from cocaine. Together, this study suggests that PRMT1 inhibition may serve as a potential therapeutic strategy for cocaine addiction.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.0246-15.2015
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2015
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  • 2
    Online Resource
    Online Resource
    Differential Roles of NR2A- and NR2B-Containing NMDA Receptors in Activity-Dependent Brain-Derived Neurotrophic Factor Gene Regulation and Limbic Epileptogenesis
    Society for Neuroscience ; 2007
    In:  The Journal of Neuroscience Vol. 27, No. 3 ( 2007-01-17), p. 542-552
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 27, No. 3 ( 2007-01-17), p. 542-552
    Abstract: Fleeting activation of NMDA receptors (NMDARs) induces long-term modification of synaptic connections and refinement of neuronal circuits, which may underlie learning and memory and contribute to pathogenesis of a diversity of neurological diseases, including epilepsy. Here, we found that NR2A and NR2B subunit-containing NMDARs were coupled to distinct intracellular signaling, resulting in differential BDNF expression and extracellular signal-regulated kinase 1/2 (ERK1/2) activation. Selective activation of NR2A-containing NMDARs increased BDNF gene expression. Activation of NR2B-containing NMDARs led to ERK1/2 phosphorylation. Furthermore, selectively blocking NR2A-containing NMDARs impaired epileptogenesis and the development of mossy fiber sprouting in the kindling and pilocarpine rat models of limbic epilepsy, whereas inhibiting NR2B-containing NMDARs had no effects in epileptogenesis and mossy fiber sprouting. Interestingly, blocking either NR2A- or NR2B-containing NMDARs decreased status epilepticus-induced neuronal cell death. The specific requirement of NR2A and its downstream signaling for epileptogenesis implicates attractive new targets for the development of drugs that prevent epilepsy in patients with brain injury.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.3607-06.2007
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2007
    detail.hit.zdb_id: 1475274-8
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  • 3
    Online Resource
    Online Resource
    Blocking the Interaction between EphB2 and ADDLs by a Small Peptide Rescues Impaired Synaptic Plasticity and Memory Deficits in a Mouse Model of Alzheimer's Disease
    Society for Neuroscience ; 2016
    In:  The Journal of Neuroscience Vol. 36, No. 47 ( 2016-11-23), p. 11959-11973
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 36, No. 47 ( 2016-11-23), p. 11959-11973
    Abstract: Soluble amyloid-β (Aβ) oligomers, also known as Aβ-derived diffusible ligands (ADDLs), are thought to be the key pathogenic factor in Alzheimer's disease (AD), but there is still no effective treatment for preventing or reversing the progression of the disease. Targeting NMDA receptor trafficking and regulation is a new strategy for early treatment of AD. Aβ oligomers have been found to bind to the fibronectin (FN) type III repeat domain of EphB2 to trigger EphB2 degradation, thereby impairing the normal functioning of NMDA receptors and resulting in cognitive deficits. Here, we identified for the first time the interaction sites of the EphB2 FN domain with ADDLs by applying the peptide array method to design and synthesize four candidate peptides (Pep21, Pep25, Pep32, and Pep63) that might be able to block the EphB2–ADDL interaction. Among them, Pep63 was found to be the most effective at inhibiting the binding between EphB2 and ADDLs. We found that Pep63 not only rescued the ADDL-induced depletion of EphB2- and GluN2B-containing NMDA receptors from the neuronal surface in cultured hippocampal neurons, but also improved impaired memory deficits in APPswe/PS1dE9 (APP/PS1) transgenic mice and the phosphorylation and surface expression of GluN2B-containing NMDA receptors in cultures. Together, these results suggest that blocking the EphB2–ADDL interaction by small interfering peptides may be a promising strategy for AD treatment. SIGNIFICANCE STATEMENT Alzheimer's disease (AD) is an age-dependent neurodegenerative disorder and amyloid β-derived diffusible ligands (ADDLs) play a key role in triggering the early cognitive deficits that constitute AD. ADDLs may bind EphB2 and alter NMDA receptor trafficking and synaptic plasticity. Here, we identified the interaction sites of the EphB2 FN domain with ADDLs for the first time to develop a small (10 aa) peptide (Pep63) capable of blocking the EphB2–ADDL interaction. We found that Pep63 not only rescued the ADDL-induced depletion of EphB2 and GluN2B-containing NMDA receptors from the neuronal surface in cultured hippocampal neurons, but also improved impaired memory deficits in APPswe/PS1dE9 (APP/PS1) transgenic mice. Our results suggest that blocking the EphB2–ADDL interaction with Pep63 may be a promising strategy for AD treatment.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1327-16.2016
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2016
    detail.hit.zdb_id: 1475274-8
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  • 4
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    Online Resource
    Astroglial Glutamate–Glutamine Shuttle Is Involved in Central Sensitization of Nociceptive Neurons in Rat Medullary Dorsal Horn
    Society for Neuroscience ; 2007
    In:  The Journal of Neuroscience Vol. 27, No. 34 ( 2007-08-22), p. 9068-9076
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 27, No. 34 ( 2007-08-22), p. 9068-9076
    Abstract: Growing evidence suggests that astroglia are involved in pain states, but no studies have tested their possible involvement in modulating the activity of nociceptive neurons per se. This study has demonstrated that the central sensitization induced in functionally identified nociceptive neurons in trigeminal subnucleus caudalis (the medullary dorsal horn) by application of an inflammatory irritant to the rat's tooth pulp can be significantly attenuated by continuous intrathecal superfusion of methionine sulfoximine (MSO; 0.1 m m ), an inhibitor of the astroglial enzyme glutamine synthetase that is involved in the glutamate–glutamine shuttle. Simultaneous superfusion of MSO and glutamine (0.25 m m ) restored the irritant-induced central sensitization. In control experiments, superfusion of either MSO or glutamine alone, or vehicle, did not produce any significant changes in neuronal properties. These findings suggest that the astroglial glutamate–glutamine shuttle is essential for the initiation of inflammation-induced central sensitization but that inhibition of astroglial function may not affect normal nociceptive processing.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2260-07.2007
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2007
    detail.hit.zdb_id: 1475274-8
    detail.hit.zdb_id: 604637-X
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  • 5
    Online Resource
    Online Resource
    Protein Kinase C Lambda Mediates Acid-Sensing Ion Channel 1a-Dependent Cortical Synaptic Plasticity and Pain Hypersensitivity
    Society for Neuroscience ; 2019
    In:  The Journal of Neuroscience Vol. 39, No. 29 ( 2019-07-17), p. 5773-5793
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 39, No. 29 ( 2019-07-17), p. 5773-5793
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.0213-19.2019
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2019
    detail.hit.zdb_id: 1475274-8
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  • 6
    Online Resource
    Online Resource
    Hypocretin-1 Potentiates NMDA Receptor-Mediated Somatodendritic Secretion from Locus Ceruleus Neurons
    Society for Neuroscience ; 2008
    In:  The Journal of Neuroscience Vol. 28, No. 12 ( 2008-03-19), p. 3202-3208
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 28, No. 12 ( 2008-03-19), p. 3202-3208
    Abstract: Our previous observations showed that several stimuli, including high-K + solution, glutamate, and voltage pulses, induce somatic noradrenaline (NA) secretion from locus ceruleus (LC) neurons. Hypocretin (orexin), a hypothalamic peptide critical for normal wakefulness, has been shown to evoke NA release from the axon terminals of LC neurons. Here, we used amperometry to test the effect of hypocretin-1 (HCRT) on NMDA receptor-mediated somatodendritic release in LC neurons. Either HCRT or NMDA applied alone dose-dependently induced somatodendritic secretion. Bath application of HCRT notably potentiated NMDA receptor-mediated somatodendritic NA release. This potentiation was blocked by SB 334867, a selective HCRT receptor (Hcrtr 1) antagonist, or bisindolylmaleimide, a specific protein kinase C (PKC) inhibitor, indicating the involvement of Hcrtr 1 and PKC. Consistent with this, phorbol 12-myristate 13-acetate, a PKC activator, mimicked the HCRT-induced potentiation. Furthermore, HCRT enhanced NMDA-induced intracellular Ca 2+ elevation via activation of Hcrtr 1 and PKC, which may contribute to HCRT-potentiated somatodendritic secretion. These results suggest that HCRT modulates LC activity not only by regulating noradrenergic input to its targets, but also by affecting noradrenergic communication in the soma and dendrites.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.4426-07.2008
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2008
    detail.hit.zdb_id: 1475274-8
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  • 7
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    Online Resource
    Activation of the Intrinsic Pain Inhibitory Circuit from the Midcingulate Cg2 to Zona Incerta Alleviates Neuropathic Pain
    Society for Neuroscience ; 2019
    In:  The Journal of Neuroscience Vol. 39, No. 46 ( 2019-11-13), p. 9130-9144
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 39, No. 46 ( 2019-11-13), p. 9130-9144
    Abstract: Neuropathic pain is one of the most common and notorious neurological diseases. The changes in cerebral structures after nerve injury and the corresponding contributions to neuropathic pain are not well understood. Here we found that the majority of glutamatergic neurons in the area 2 of midcingulate cortex (MCC Cg2 Glu ) were inhibited by painful stimulation in male mice. Optogenetic manipulation revealed that these neurons were tonically involved in the inhibitory modulation of multimodal nociception. We further identified the projections to GABAergic neurons in the zona incerta (ZI GABA ) mediated the pain inhibitory role. However, MCC Cg2 Glu became hypoactive after nerve injury. Although a brief activation of the MCC Cg2 Glu to ZI GABA circuit was able to relieve the aversiveness associated with spontaneous ongoing pain, consecutive activation of the circuit was required to alleviate neuropathic allodynia. In contrast, glutamatergic neurons in the area 1 of MCC played opposite roles in pain modulation. They became hyperactive after nerve injury and only consecutive inhibition of their activity relieved allodynia. These results demonstrate that MCC Cg2 Glu constitute a component of intrinsic pain inhibitory circuitry and their hypoactivity underlies neuropathic pain. We propose that selective and persistent activation of the MCC Cg2 Glu to ZI GABA circuit may serve as a potential therapeutic strategy for this disease. SIGNIFICANCE STATEMENT Glutamatergic neurons in the area 2 of midcingulate cortex (MCC Cg2 Glu ) are tonically involved in the intrinsic pain inhibition via projecting to GABAergic neurons in the zona incerta. They are hypoactive after nerve injury. Selective activation of the circuit compensates the reduction of its analgesic strength and relieves neuropathic pain. Therefore, MCC Cg2 Glu and the related analgesic circuit may serve as therapeutic targets for neuropathic pain. In contrast, MCC Cg1 Glu have an opposite role in pain modulation and become hyperactive after nerve injury. The present study provides novel evidence for the concept that neuropathic pain is associated with the dysfunction of endogenous pain modulatory system and new perspective on the treatment of neuropathic pain.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1683-19.2019
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2019
    detail.hit.zdb_id: 1475274-8
    detail.hit.zdb_id: 604637-X
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  • 8
    Online Resource
    Online Resource
    Facilitation of Behavioral and Cortical Emergence from Isoflurane Anesthesia by GABAergic Neurons in Basal Forebrain
    Society for Neuroscience ; 2023
    In:  The Journal of Neuroscience Vol. 43, No. 16 ( 2023-04-19), p. 2907-2920
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 43, No. 16 ( 2023-04-19), p. 2907-2920
    Abstract: General anesthesia shares many similarities with natural sleep in behavior and electroencephalogram (EEG) patterns. The latest evidence suggests that general anesthesia and sleep–wake behavior may share overlapping neural substrates. The GABAergic neurons in the basal forebrain (BF) have recently been demonstrated to play a key role in controlling wakefulness. It was hypothesized that BF GABAergic neurons may participate in the regulation of general anesthesia. Here, using in vivo fiber photometry, we found that the activity of BF GABAergic neurons was generally inhibited during isoflurane anesthesia, having obviously decreased during the induction of anesthesia and being gradually restored during the emergence from anesthesia, in Vgat-Cre mice of both sexes. Activation of BF GABAergic neurons with chemogenetic and optogenetic approaches decreased sensitivity to isoflurane, delayed induction, and accelerated emergence from isoflurane anesthesia. Optogenetic activation of BF GABAergic neurons decreased EEG δ power and the burst suppression ratio (BSR) during 0.8% and 1.4% isoflurane anesthesia, respectively. Similar to the effects of activating BF GABAergic cell bodies, photostimulation of BF GABAergic terminals in the thalamic reticular nucleus (TRN) also strongly promoted cortical activation and behavioral emergence from isoflurane anesthesia. Collectively, these results showed that the GABAergic BF is a key neural substrate for general anesthesia regulation that facilitates behavioral and cortical emergence from general anesthesia via the GABAergic BF-TRN pathway. Our findings may provide a new target for attenuating the depth of anesthesia and accelerating emergence from general anesthesia. SIGNIFICANCE STATEMENT The basal forebrain (BF) is a key brain region controlling sleep–wake behavior. Activation of GABAergic neurons in the BF potently promotes behavioral arousal and cortical activity. Recently, many sleep–wake-related brain structures have been reported to participate in the regulation of general anesthesia. However, it is still unclear what role BF GABAergic neurons play in general anesthesia. In this study, we aim to reveal the role of BF GABAergic neurons in behavioral and cortical emergence from isoflurane anesthesia and elucidate the underlying neural pathways. Understanding the specific role of BF GABAergic neurons in isoflurane anesthesia would improve our understanding of the mechanisms of general anesthesia and may provide a new strategy for accelerating emergence from general anesthesia.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
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    DOI: 10.1523/JNEUROSCI.0628-22.2023
    DOI: 10.1523/JNEUROSCI.0628-22.2023.ed1
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f1-1
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f2-1
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f2-2
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f3-1
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f3-2
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f3-3
    DOI: 10.1523/JNEUROSCI.0628-22.2023.video.1
    DOI: 10.1523/JNEUROSCI.0628-22.2023.video.2
    DOI: 10.1523/JNEUROSCI.0628-22.2023.video.3
    DOI: 10.1523/JNEUROSCI.0628-22.2023.video.4
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f5-1
    DOI: 10.1523/JNEUROSCI.0628-22.2023.f5-2
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2023
    detail.hit.zdb_id: 1475274-8
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  • 9
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    In Vivo Expansion of Regulatory T Cells with IL-2/IL-2 Antibody Complex Protects against Transient Ischemic Stroke
    Society for Neuroscience ; 2018
    In:  The Journal of Neuroscience Vol. 38, No. 47 ( 2018-11-21), p. 10168-10179
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 38, No. 47 ( 2018-11-21), p. 10168-10179
    Abstract: Regulatory T cells (Tregs) are known to protect against ischemic stroke. However, the low frequency of Tregs restricts their clinical utility. This study investigated whether expanding the number of Tregs in vivo with the IL-2/IL-2 antibody complex (IL-2/IL-2Ab) could improve stroke outcomes and further elaborated the mechanisms of protection in male mice. C57BL/6 mice received IL-2/IL-2Ab or isotype IgG (IsoAb) intraperitoneally for 3 d before (pretreatment) or starting 2 h after (posttreatment) 60 min middle cerebral artery occlusion (MCAO). IL-2/IL-2Ab selectively increased the number of Tregs in the blood, spleen, and lymph nodes. The IL-2/IL-2Ab treatment significantly reduced infarct volume, inhibited neuroinflammation, and improved sensorimotor functions, as manifested by rotarod test and foot fault test, compared with IsoAb-treated stroke mice. Treg depletion was then achieved by diphtheria toxin (DT) injection into transgenic mice expressing the DT receptor under the control of the Foxp3 promoter (DTR mice). The depletion of Tregs completely eliminated IL-2/IL-2Ab-afforded neuroprotection. Interestingly, adoptive transfer of Tregs collected from IL-2/IL-2Ab-treated mice demonstrated more potent neuroprotection than an equal number of Tregs prepared from IsoAb-treated mice, suggesting that IL-2/IL-2Ab not only elevated Treg numbers, but also boosted their functions. Mechanistically, IL-2/IL-2Ab promoted the expression of CD39 and CD73 in expanded Tregs. CD73 deficiency diminished the protective effect of IL-2/IL-2Ab-stimulated Tregs in stroke mice. The results show that IL-2/IL-2Ab expands Tregs in vivo and boosts their immunomodulatory function. The activation of CD39/CD73 signaling in Tregs may participate as a potential mechanism underlying IL-2/IL-2Ab-afforded neuroprotection against ischemic brain injury. SIGNIFICANCE STATEMENT Regulatory T cells (Tregs) are known to protect against ischemic stroke. However, the low frequency of Tregs restricts their clinical utility. This study reported that systemic administration of the IL-2/IL-2 antibody complex (IL-2/IL-2Ab) robustly and selectively expanded the number of Tregs after stroke. IL-2/IL-2Ab pretreatment or posttreatment significantly improved stroke outcomes in a rodent model of ischemic stroke. We further discovered that IL-2/IL-2Ab not only elevated Treg numbers, but also boosted their functions and enhanced the expression of CD39 and CD73. Using CD73-deficient mice, we confirmed the importance of CD73 in the protective effect of IL-2/IL-2Ab-stimulated Tregs in stroke mice. These results shed light on IL-2/IL-2Ab as a clinically feasible immune therapy to boost endogenous Treg responses and ameliorate ischemic brain injury.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    URL: Article
    DOI: 10.1523/JNEUROSCI.3411-17.2018
    DOI: 10.1523/JNEUROSCI.3411-17.2018.t9-1
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2018
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  • 10
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    The Modulatory Effect of Motor Cortex Astrocytes on Diabetic Neuropathic Pain
    Society for Neuroscience ; 2021
    In:  The Journal of Neuroscience Vol. 41, No. 24 ( 2021-06-16), p. 5287-5302
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 41, No. 24 ( 2021-06-16), p. 5287-5302
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1523/JNEUROSCI.2566-20.2021
    DOI: 10.1523/JNEUROSCI.2566-20.2021.f2-1
    DOI: 10.1523/JNEUROSCI.2566-20.2021.f3-1
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2021
    detail.hit.zdb_id: 1475274-8
    detail.hit.zdb_id: 604637-X
    SSG: 12
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